Exposure to Air Pollution Exacerbates Inflammation in Rats with Preexisting COPD

Abstract

Particulate matter with an aerodynamic diameter equal or less than 2.5 micrometers (PM2.5) is associated with the development of chronic obstructive pulmonary disease (COPD). The mechanisms by which PM2.5 accelerates disease progression in COPD are poorly understood. In this study, we aimed to investigate the effect of PM2.5 on lung injury in rats with hallmark features of COPD. Cardinal features of human COPD were induced in a rat model by repeated cigarette smoke inhalation and bacterial infection for 8 weeks. Then, from week 9 to week 16, some of these rats with COPD were subjected to real-time concentrated atmospheric PM2.5. Lung function, pathology, inflammatory cytokines, oxidative stress, and mucus and collagen production were measured. As expected, the COPD rats had developed emphysema, inflammation, and deterioration in lung function. PM2.5 exposure resulted in greater lung function decline and histopathological changes, as reflected by increased Mucin (MUC) 5ac, MUC5b, Collagen I, Collagen III, and the profibrotic cytokine α-smooth muscle-actin (SMA), transforming growth factor- (TGF-) β1 in lung tissues. PM2.5 also aggravated inflammation, increasing neutrophils and eosinophils in bronchoalveolar lavage fluid (BALF) and cytokines including Interleukin- (IL-) 1β, granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-4. The likely mechanism is through oxidative stress as antioxidants levels were decreased, whereas oxidants were increased, indicating a detrimental shift in the oxidant-antioxidant balance. Altogether, these results suggest that PM2.5 exposure could promote the development of COPD by impairing lung function and exacerbating pulmonary injury, and the potential mechanisms are related to inflammatory response and oxidative stress.

Antiflammatory activity and potential dermatological applications of characterized humic acids from a lignite and a green compost

“…The most common air pollutants comprise polycyclic aromatic hydrocarbons (PAHs), volatile organic compounds (VOCs, e.g., benzene), particulate matter (PM, most commonly PM2.5 and PM10), gaseous pollutants, (carbon-monoxide, nitric oxides, sulphur oxide, ozone, heavy metals) and indoor pollutants, as solid fuels consumption 8 . Although the molecular mechanisms relating air pollutions to skin diseases are not yet fully understood, several in vivo studies have highlighted the occurrence and prominence of the inflammatory state as a common factor of these conditions 9 . Particularly, the activation of a multiprotein complex called inflammasome, has been hypothesized to trigger the inflammatory responses by promoting the maturation of proinflammatory cytokines 10 .…”

Effect of urban air pollution on CRP and coagulation: a study on inpatients with acute exacerbation of chronic obstructive pulmonary disease

“…PM contains volatile mixtures of numerous heavy metals, organic compounds, and carcinogens that interact with in vivo cellular mechanisms and induce vascular damage, including endothelium inflammation, development of atherosclerosis, lipid peroxidation, alterations in cytokines and acute phase protein levels (such as CRP), and procoagulant responses [ 41 , 42 ]. The mechanisms by which PM accelerates disease progression in COPD involve changes in the prooxidant-antioxidant balance [ 43 ]. Air PM increases the levels of reactive oxygen species (ROS), disrupts cell homeostasis, or activates the redox-sensitive signaling pathway to activate inflammatory cells, pro-inflammatory gene expression, and cytokine production [ 44 ].…”

Effects of PM2.5 on Chronic Airway Diseases: A Review of Research Progress

“…Repeated PM 2.5 also resulted in decreased pulmonary function and emphysema, even at a lower level [31]. PM 2.5 dose-dependently upregulates the expression of matrix metalloproteinase (MMP-9), MMP-12, fibronectin, collagen, and transforming growth factor (TGF)-β1, in which the increased protease activity is highly related to airway remodeling and development of emphysema in COPD [32]. Of note, PM 2.5 exposure could significantly worsen cigarette smoking (CS)-induced changes in COPD, suggesting that PM 2.5 and CS may synergistically promote the occurrence and the development of COPD.…”